Acute Brain Research Articles

ALS-like pathology diminishes swelling of spinal astrocytes in the SOD1 animal model.

Astrocytes are crucial for the functioning of the nervous system as they maintain the ion homeostasis via volume regulation. Pathological states, such as amyotrophic lateral sclerosis (ALS), affect astrocytes and might even cause a loss of such functions. In this study, we examined astrocytic swelling/volume recovery in both the brain and spinal cord of the SOD1 animal model to determine the level of their impairment caused by the ALS-like pathology. Astrocyte volume changes were measured in acute brain or spinal cord slices during and after exposure to hyperkalemia. We then compared the results with alterations of extracellular space (ECS) diffusion parameters, morphological changes, expression of the Kir4.1 channel and the potassium concentration measured in the cerebrospinal fluid, to further disclose the link between potassium and astrocytes in the ALS-like pathology. Morphological analysis revealed astrogliosis in both the motor cortex and the ventral horns of the SOD1 spinal cord. The activated morphology of SOD1 spinal astrocytes was associated with the results from volume measurements, which showed decreased swelling of these cells during hyperkalemia. Furthermore, we observed lower shrinkage of ECS in the SOD1 spinal ventral horns. Immunohistochemical analysis then confirmed decreased expression of the Kir4.1 channel in the SOD1 spinal cord, which corresponded with the diminished volume regulation. Despite astrogliosis, cortical astrocytes in SOD1 mice did not show alterations in swelling nor changes in Kir4.1 expression, and we did not identify significant changes in ECS parameters. Moreover, the potassium level in the cerebrospinal fluid did not deviate from the physiological concentration. The results we obtained thus suggest that ALS-like pathology causes impaired potassium uptake associated with Kir4.1 downregulation in the spinal astrocytes, but based on our data from the cortex, the functional impairment seems to be independent of the morphological state.

The Loss of Temporal Muscle Volume is Associated with Poor Outcome in Patients with Subarachnoid Hemorrhage: An Observational Cohort Study

BackgroundIntensive care unit (ICU) acquired weakness is a major contributor to poor functional outcome of ICU patients. Quantification of temporal muscle volume assessed on routine computed tomography (CT) scans may serve as a biomarker for muscle wasting in patients suffering from acute brain injury.MethodsThis is a retrospective analysis of prospectively collected data. Temporal muscle volume was assessed on head CT scans of consecutive patients with spontaneous subarachnoid hemorrhage within prespecified time frames (on admission, then weekly ± 2 days). Whenever possible, temporal muscle volume was assessed bilaterally and averaged for the analysis. Poor functional outcome was defined as a 3-month modified Rankin Scale Score ≥ 3. Statistical analysis was performed using generalized estimating equations to handle repeated measurements within individuals.ResultsThe analysis comprised 110 patients with a median Hunt & Hess score of 4 (interquartile range 3–5). Median age was 61 (50–70) years, 73 patients (66%) were women. Baseline temporal muscle volume was 18.5 ± 0.78 cm3 and significantly decreased over time (p < 0.001) by a mean of 7.9% per week. Higher disease severity (p = 0.002), hydrocephalus (p = 0.020), pneumonia (p = 0.032), and bloodstream infection (p = 0.015) were associated with more pronounced muscle volume loss. Patients with poor functional outcome had smaller muscle volumes 2 and 3 weeks after subarachnoid hemorrhage compared with those with good outcome (p = 0.025). The maximum muscle volume loss during ICU stay was greater in patients with poor functional outcome (− 32.2% ± 2.5% vs. − 22.7% ± 2.5%, p = 0.008). The hazard ratio for poor functional outcome was 1.027 (95% confidence interval 1.003–1.051) per percent of maximum muscle volume loss.ConclusionsTemporal muscle volume, which is easily assessable on routine head CT scans, progressively decreases during the ICU stay after spontaneous subarachnoid hemorrhage. Because of its association with disease severity and functional outcome, it may serve as a biomarker for muscle wasting and outcome prognostication.

Neurogenically Originated Inflammatory Response Syndrome: Role in the Neurocritical Patient

The systemic inflammatory response syndrome (SIRS) consists of an inflammatory phenomenon as a response of the immune system against infections, as well as non-infectious injuries, which includes manifestations that affect multiple organs, among which hyperthermia or hypothermia, leukopenia or leukocytosis, tachycardia, and tachypnea. SIRS accompanies different acute brain and spinal cord injuries, including subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord trauma, traumatic brain injury, and status epilepticus. We suggest a new term for this condition neurogenically originated systemic inflammatory response syndrome (NoSIRS). NIRS can be considered a new syndrome associated with pathological neurological conditions. However, more research is needed to figure out the true severity of this clinical picture and also figure out the best way to treat this condition.

The Value of First-Order Features Based on the Apparent Diffusion Coefficient Map in Evaluating the Therapeutic Effect of Low-Intensity Pulsed Ultrasound for Acute Traumatic Brain Injury With a Rat Model.

PurposeIn order to evaluate the neuroprotective effect of low-intensity pulsed ultrasound (LIPUS) for acute traumatic brain injury (TBI), we studied the potential of apparent diffusion coefficient (ADC) values and ADC-derived first-order features regarding this problem.MethodsForty-five male Sprague Dawley rats (sham group: 15, TBI group: 15, LIPUS treated: 15) were enrolled and underwent magnetic resonance imaging. Scanning layers were acquired using a multi-shot readout segmentation of long variable echo trains (RESOLVE) to decrease distortion. The ultrasound transducer was applied to the designated region in the injured cortical areas using a conical collimator and was filled with an ultrasound coupling gel. Regions of interest were manually delineated in the center of the damaged cortex on the diffusion weighted images (b = 800 s/mm2) layer by layer for the TBI and LIPUS treated groups using the open-source software ITK-SNAP. Before analysis and modeling, the features were normalized using a z-score method, and a logistic regression model with a backward filtering method was employed to perform the modeling. The entire process was completed using the R language.ResultsDuring the observation time, the ADC values ipsilateral to the trauma in the TBI and LIPUS groups increased rapidly up to 24 h. After statistical analysis, the 10th percentile, 90th percentile, mean, skewness, and uniformity demonstrated a significant difference among three groups. The receiver operating characteristic curve (ROC) analysis shows that the combined LR model exhibited the highest area under the curve value (AUC: 0.96).ConclusionThe combined LR model of first-order features based on the ADC map can acquire a higher diagnostic performance than each feature only in evaluating the neuroprotective effect of LIPUS for TBI. Models based on first-order features may have potential value in predicting the therapeutic effect of LIPUS in clinical practice in the future.

Dysregulation of Astrocytic Glutamine Transport in Acute Hyperammonemic Brain Edema.

Acute liver failure (ALF) impairs ammonia clearance from blood, which gives rise to acute hyperammonemia and increased ammonia accumulation in the brain. Since in brain glutamine synthesis is the only route of ammonia detoxification, hyperammonemia is as a rule associated with increased brain glutamine content (glutaminosis) which correlates with and contributes along with ammonia itself to hyperammonemic brain edema-associated with ALF. This review focuses on the effects of hyperammonemia on the two glutamine carriers located in the astrocytic membrane: Slc38a3 (SN1, SNAT3) and Slc7a6 (y + LAT2). We emphasize the contribution of the dysfunction of either of the two carriers to glutaminosis- related aspects of brain edema: retention of osmotically obligated water (Slc38a3) and induction of oxidative/nitrosative stress (Slc7a6). The changes in glutamine transport link glutaminosis- evoked mitochondrial dysfunction to oxidative-nitrosative stress as formulated in the “Trojan Horse” hypothesis.

Diagnosis and Management of Geriatric Patients’ Delirium

&lt;p&gt;譫妄症是急性腦功能受損的一種表現,同時譫妄症也是一種以意識障礙為主的 急性症狀;發生譫妄症之後往往會造成龐大的醫療花費(例如延長住院天數),且 臨床上容易被忽略,造成老年疾病的預後不佳,更可能進一步造成病患的死亡,是 病患安全重要指標;基於其病因的多重因子特性,且與其他老年病症候群(如:跌 倒、失禁)的高度聯結性,因此在處置上也需要多方向並進的治療,針對譫妄症的 完善處理,可明顯改善病患預後,並增進醫療的品質。本文為敘述性文獻回顧,以 老年症候群及急性譫妄症處置為關鍵字,藉由文獻搜尋並整理譫妄症的診斷與處 置,期望可作為醫療人員遭遇病患時不只使用約束帶或藥物,可以有更周全的評估 與治療。&lt;/p&gt; &lt;p&gt;&amp;nbsp;&lt;/p&gt;&lt;p&gt;Delirium is a manifestation of acute impaired brain function. At the same time, delirium is also an acute sign/symptom dominated by disturbances in consciousness. The occurrence of delirium often causes huge medical expenses (ex: prolonged hospitalization days) and often results in poor prognoses for senile diseases. It is more likely to cause further death of patients, which is an important indicator of patient safety, based on its multifactorial etiology and high connectivity with other senile diseases (such as falls, incontinence, etc.). It is also necessary for patients to receive multi-directional treatment that can signifi- cantly improve the prognoses of patients and improve the quality of medication. This article is a narrative literature review with geriatric syndrome and acute delirium management as the keywords. Through a literature survey and sorting out the diagnosis and treatment of delirium, it is hoped that medical staff can not only use restraint bands or sedative drugs when encountering patients, but also provide comprehensive assessment, evaluation and treatment.&lt;/p&gt; &lt;p&gt;&amp;nbsp;&lt;/p&gt;

Analysis of the risk factors for intraoperative acute diffuse brain swelling in patients with isolated traumatic acute subdural haematomas

BackgroundThe purpose of this retrospective study was to investigate the risk factors for intraoperative acute diffuse brain swelling in patients with isolated traumatic acute subdural haematomas (ASDH).MethodsA total of 256 patients who underwent decompressive craniectomy for isolated traumatic ASDH between April 2013 and December 2020 were included. We evaluated the risk factors for intraoperative acute diffuse brain swelling using a multivariate logistic regression analysis.ResultsThe incidence of intraoperative acute diffuse brain swelling in patients with isolated traumatic ASDH was 21.88% (56/256). Dilated pupils (OR = 24.78), subarachnoid haemorrhage (OR = 2.41), and the time from injury to surgery (OR = 0.32) were independent risk factors for intraoperative acute diffuse brain swelling, while no independent associations were observed between these risk factors and sex, age, the mechanism of injury, the Glasgow Coma Scale score, site of haematoma, thickness of haematoma, midline shift and the status of the basal cistern, although the mechanism of injury, the Glasgow Coma Scale score and the status of the basal cistern were correlated with the incidence of intraoperative acute diffuse brain swelling in the univariate analyses.ConclusionsThis study identified the risk factors for intraoperative acute diffuse brain swelling in patients with isolated traumatic ASDH. An increased risk of intraoperative acute diffuse brain swelling occurs in patients with bilaterally dilated pupils, subarachnoid haemorrhage and a shorter time from injury to surgery. These findings should help neurosurgeons obtain information before surgery about intraoperative acute diffuse brain swelling in patients with isolated traumatic ASDH.

Serum metabolome associated with severity of acute traumatic brain injury

Complex metabolic disruption is a crucial aspect of the pathophysiology of traumatic brain injury (TBI). Associations between this and systemic metabolism and their potential prognostic value are poorly understood. Here, we aimed to describe the serum metabolome (including lipidome) associated with acute TBI within 24 h post-injury, and its relationship to severity of injury and patient outcome. We performed a comprehensive metabolomics study in a cohort of 716 patients with TBI and non-TBI reference patients (orthopedic, internal medicine, and other neurological patients) from the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) cohort. We identified panels of metabolites specifically associated with TBI severity and patient outcomes. Choline phospholipids (lysophosphatidylcholines, ether phosphatidylcholines and sphingomyelins) were inversely associated with TBI severity and were among the strongest predictors of TBI patient outcomes, which was further confirmed in a separate validation dataset of 558 patients. The observed metabolic patterns may reflect different pathophysiological mechanisms, including protective changes of systemic lipid metabolism aiming to maintain lipid homeostasis in the brain.

Assaying activity-dependent arteriole and capillary responses in brain slices.

.SignificanceNeurovascular coupling (NVC) is the process that increases cerebral blood flow in response to neuronal activity. NVC is orchestrated by signaling between neurons, glia, and vascular cells. Elucidating the mechanisms underlying NVC at different vascular segments and in different brain regions is imperative for understanding of brain function and mechanisms of dysfunction.AimOur goal is to describe a protocol for concurrently monitoring stimulation-evoked neuronal activity and resultant vascular responses in acute brain slices.ApproachWe describe a step-by-step protocol that allows the study of endogenous NVC mechanisms engaged by neuronal activity in a controlled, reduced preparation.ResultsThis ex vivo NVC assay allows researchers to disentangle the mechanisms regulating the contractile responses of different vascular segments in response to neuronal firing independent of flow and pressure mediated effects from connected vessels. It also enables easy pharmacological manipulations in a simplified, reduced system and can be combined with imaging or broader electrophysiology techniques to obtain multimodal data during NVC.ConclusionsThe ex vivo NVC assay will facilitate investigations of cellular and molecular mechanisms that give rise to NVC and should serve as a valuable complement to in vivo imaging methods.

Cerebral stroke in patients with malignant neoplasms (literature review)

The article reflects the significant domestic and foreign literature data result on the development of cerebral stroke against the background of malignant neoplasm analysis and the identification of specific risk factors for brain acute vascular lesions in patients with cancer.Aim. Literature data analysis on cerebral stroke and specific risk factors for its development in patients with malignant neoplasms.Materials and methods. Domestic and foreign literature sources on the influence of oncopathology on the cerebral stroke occurrence subject were studied.Results. The presence of a malignant neoplasm seems to be an independent risk factor for death in patients with cerebral infarction, and its risk is the same in men and women. The main link in acute ischemic brain injury in patients with malignant neoplasms is the tissue factor expression that triggers a coagulation cascade with an increase in the level of D-dimer and other fibrin degradation products. Stroke risk is highest in the first 3 months after the detection of the tumor and significantly decreases by the year.Conclusions. Scientific research of the oncopathology on the cerebral stroke development influence mainly concern the hemostasis study without assessing its platelet component and the oncopathology type in this category of patients, but do not sufficiently reflect the structure of acute cerebrovascular accidents. Literature analysis showed the absence of studies on the relationship between the strokes’ frequency and histological and immunohistochemical data.

Abstract TP242: The Suppression Of Leukocyte Rolling Via Blocking P-selectin After Stroke Is Not Sustained In Mice With Type 2 Diabetes

Introduction: Diabetes is associated with worse stroke outcome, yet the mechanism contributing to a more severe ischemic brain injury is not well understood. Neutrophils invade the cerebral veins as early as 30 minutes after stroke and play a major role in acute ischemic brain injury and thrombosis. Leukocyte rolling on the activated endothelium is an early event of transendothelial migration and parenchymal infiltration of leukocytes including neutrophils, which involves p-selectin. The current study sought to determine the effect of blocking p-selectin in reducing leukocyte rolling in the cerebral vessels of diabetic mice after stroke. Methods: Stroke was induced in 4-month old diabetic db/db and control db/+ mice via middle cerebral artery occlusion (MCAO). P-selectin blocking antibody (P-aby) was administered intravenously 30 min after MCAO at 20 mg/kg. Adherent or rolling leukocytes was quantified at baseline before MCAO and after ischemic reperfusion by repeated 2-photon microscope imaging with fluorescent tracers. Infiltrating neutrophils and plasma soluble p-selectin were determined via FACS and ELISA, respectively. Results: Leukocyte rolling was immediate detected in the veins 1 hr after reperfusion and significantly increased 1d after MCAO in both genotypes of mice. Rolling tended to last days longer in the db/db compared to db/+ mice, and was often seen in the arterioles of the former but not in the latter mice. Increased infiltration of neutrophils was detected in db/db compared to db/+ brain parenchyma 1-3 ds after MCAO by FACS. Three to 5 fold-reduction in rolling by was detected 1 hr after reperfusion in both genotypes following P-aby treatment. However, rolling resumed in db/db mice 1 d after MCAO and antibody treatment, compared to a sustained suppression of rolling seen in the db/+ mice till days later. Elevated soluble p-selectin was also detected in the plasma of db/db compared to db/+ mice. Conclusions: Stroke-induced leukocyte rolling was only temporarily suppressed by P-selectin blocking antibody in db/db mice. Ongoing studies will determine the effect of P-selectin blocking on microthrombi formation, cerebral blood flow, neuroprotection and the role of soluble p-selectin in dampening the treatment effect.

Effectiveness and Safety of Early Tranexamic Acid in Patients with Acute Traumatic Brain Injuries

Effectiveness and Safety of Early Tranexamic Acid in Patients with Acute Traumatic Brain Injuries

Active rehabilitation intervention following acute mild traumatic brain injury: A systematic review

Active rehabilitation intervention following acute mild traumatic brain injury: A systematic review

Intradermal injection of icariin-HP-β-cyclodextrin improved traumatic brain injury via the trigeminal epineurium-brain dura pathway

The lower bioavailability after oral administration limited icariin applications in central nervous system. Icariin/HP-β-cyclodextrin (HP-β-CD) inclusion complex was prepared for acute severe opening traumatic brain injury (TBI) via facial intradermal (i.d.) in the mystacial pad. After fluid percussion-induced TBI, icariin/HP-β-CD at 0.4 mg/kg i.d. preserved more neurons and oligodendrocytes than intranasal injection (i.n.) or intravenous injection via tail vein (i.v.) and decreased microglia and astrocyte activation. Icariin/HP-β-CD i.d. reduced apoptosis in cortical penumbra while i.n. and i.v. showed weak or no effects. Icariin/HP-β-CD i.d. reduced Evans blue leakage and altered CD34, ZO-1, Claudin-5, and beta-catenin expression after TBI. Moreover, icariin/HP-β-CD promoted human umbilical vein endothelial cells proliferation. Thus, Icariin/HP-β-CD i.d. improved TBI, including blood–brain barrier opening. Fluorescein 5-isothiocyanate (FITC) and 3,3'-Dioctadecyloxacarbocyanine perchlorate (DiOC18(3)) mimic HP-β-CD and icariin respectively. FITC and DiOC18(3) were similarly delivered to trigeminal epineurium, perineurium and perivascular spaces or tissues, caudal dura mater, and scattered in trigeminal fasciculus, indicating that icariin/HP-β-CD was delivered to the brain via trigeminal nerve-dura mater-brain pathways. In sum, intradermal injection in mystacial pad might deliver icariin/HP-β-CD to the brain and icariin/HP-β-CD improved acute severe opening TBI.

Acute Brain and Lung Failure as the Major Risk Factor of Worse Outcomes in Sepsis: A Retrospective Population-Based Cohort Study

Acute Brain and Lung Failure as the Major Risk Factor of Worse Outcomes in Sepsis: A Retrospective Population-Based Cohort Study

Структура судомного синдрому в пацієнтів із черепно-мозковою травмою в гострому періоді

Актуальність. Вивчення структури епілептичних нападів, часу їх появи, зв’язку з характером черепно­мозкової травми дозволяє виявити групу потерпілих, які потребуватимуть невідкладної хірургічної корекції їх стану, профілактичного призначення протиепілептичних препаратів, а також уточнити вплив епілептичних нападів на наслідки травми. Мета: вивчити структуру епілептичних нападів у гострому періоді черепно­мозкової травми для оптимізації діагностичних і лікувальних заходів у відповідної категорії пацієнтів. Матеріали та методи. Проведено клінічне, інструментальне обстеження й проаналізовано результати лікування 779 хворих із черепно­мозковою травмою, у яких при надходженні та/або перебуванні в стаціонарі мали місце епілептичні напади. Середній вік пацієнтів становив 35,5 ± 7,8 року. Більшість спостережень — кримінальна травма — 320 хворих (41,1 %), у 272 осіб травма була наслідком дорожньо­транспортної пригоди (34,9 %), 109 хворих отримали травму при падінні з висоти власного росту (13,9 %), у 78 хворих обставини травми були невідомі (10,0 %). Результати. Епілептичні напади виникають у 8,4 % хворих у гострому періоді черепно­мозкової травми. У 81,4 % мали місце негайні епілептичні напади, у 15,7 % — ранні епілептичні напади, у 2,9 % — пізні епілептичні напади. Для негайних і ранніх епілептичних нападів характерними були парціальні епілептичні судоми, у структурі пізніх епілептичних нападів у гострому періоді черепно­мозкової травми переважали генералізовані епілептичні напади. 422 хворих (54,2 %) прооперовано в ургентному порядку. Хірургічне лікування після попередньої консервативної терапії виконано у 232 хворих (29,8 %). Консервативна терапія проведена в 125 пацієнтів (16,0 %). Висновки. Неврологічне обстеження хворих з епілептичними нападами в гострому періоді черепно­мозкової травми обов’язково повинне доповнюватися проведенням комп’ютерної томографії головного мозку, незалежно від рівня порушення свідомості пацієнта. Екстрене хірургічне втручання в таких хворих, спрямоване на усунення прогресуючого дислокаційного синдрому, часто є основним методом лікування. Терапія протиепілептичними препаратами повинна проводитись після появи одиничного епілептичного нападу протягом короткого періоду часу, за наявності неспровокованих епілептичних нападів і їх повторюваності прийом протиепілептичних препаратів повинен бути тривалим.

Diffusion weight magnetic resonance imaging analisys with rapid software appication in symptomatic carotid stenosis revascularization

Abstract Objectives The aim of this study was to evaluate whether the extension of preoperative neuroradiological lesions assessed by magnetic resonance imaging (MRI) with Diffusion Weighted sequences (DWI) and Rapid processing of Perfusion and Diffusion software are potentially related to post-operative neurological outcome in patients with symptomatic carotid stenosis (SCS) treated by carotid endarterectomy (CEA). Methods From January 2010 to June 2020, data from 134 consecutive patients affected by SCS, presenting with transient ischemic attack (TIA), and minor or moderate stroke, and submitted to urgent CEA in a single academic center, were prospectively collected and reviewed. All SCS patients underwent independent neurological evaluation, duplex ultrasound scan, computed tomographic angiography, and DW-MRI with RAPID evaluation. RAPID evaluation was performed to assess the volume of acute ischemic brain lesion (IBL); through this method it is possible to obtain the identification of the ischemic core milliliters (mL). According with clinical presentation, and imaging studies analysis CEA endarterectomies were performed within 48 hours, within 14 days or after 14 days from symptoms onset. Outcomes for presented analysis were the post-operative new neurological event, and deathat follow-up. Timing of CEA and IBL volume at RAPID evaluation were considered as risk factor potentially influencing outcomes. Results Among all the 134 enrolled patients, 68 patients (50.7%) presented with TIA, 49 (36.6%) with a minor Stroke, and 17 (12.7%) with a moderate Stroke. No intraoperative death occurred in any group. Overall, 6 (4.4%) new neurological events were noted in this series, 1 minor stroke (0.7%), and 5 TIAs (3.7%). One-hundred-fifteen (86%) underwent surgery within 14 days from neurological symptoms onset (Urgent patients – U), and 19 (14%) after 14 days (Delayed patients – D); U patients were also divided in two subgroups U1 47/115 patients (35%) submitted to CEA within 48 hours from symptoms onset, and U2 68/115 patients (51%) after 48 hours. No neurological complications were noted in group D, while 5 new adverse events occurred in U1, and 1 in U2 (p=0.01). Results from MRI with DWI sequences performed in 100/134 patients (74.6%) showed positive preoperative diffusion in 62 patients. The RAPID processing ascribed a 0 value, for punctiform lesions, and a value from 2 to 77 ml for single acute lesions; average volume lesion volume was 8.6 mL. Patients were then divided into two groups according to IBL volume: 84 &amp;lt;10 ml, and 16≥10 mL. Incidence of new neurological events was significantly higher in &amp;gt;10ml group (18.7% vs 3.6%; p=0.02). Conclusion Our experience seems to suggest that the optimal time for SCS revascularization is between 48 hours and 14 days. Moreover, IBL volume &amp;gt;10ml might greatly increase risk of postoperative adverse events occurrence. Funding Acknowledgement Type of funding sources: None.

Changes of Blood Leukocyte and Blood Glucose in Patients with Acute Craniocerebral Trauma and Nursing Effect

Acute craniocerebral injury is one of the most common injury types, and its mortality rate ranks first among all kinds of injuries. The changes of white blood cells and blood glucose play an important role in the treatment and nursing of patients. The purpose of this study is to analyze the changes of white blood cells and blood glucose in patients with acute craniocerebral trauma and nursing effect. In this study, 65 patients with craniocerebral injury admitted to the Department of Neurosurgery of our hospital from January 2017 to September 2019 were selected as the research objects. After admission, appropriate nutritional treatment was given according to the condition of patients. Blood samples were collected on fasting in the morning of 2, 8 and 15 days after admission, while those in the control group were collected by fasting vein for detection of white blood cells, blood glucose, blood lipid, blood uric acid and other indicators. There was no significant difference in the number of neutrophils in each group (P &lt; 0.05, P &lt; 0.05, P &lt; 0.05, P &lt; 0.05, P &lt; 0.05). After acute traumatic brain injury, the white blood cells and blood glucose of patients increased, and the more severe the degree of brain injury, the higher the white blood cell count and blood glucose. This study will contribute to the analysis of white blood cell and blood glucose changes and nursing care of patients with craniocerebral injury.

Effects of Hyperbaric Oxygen Therapy on Serum Adhesion Molecules, and Serum Oxidative Stress in Patients with Acute Traumatic Brain Injury.

Background: Serum concentrations of adhesion molecules and oxidative stress is thought to participate in the pathobiology of secondary brain injury after acute traumatic brain injury (TBI). We aimed to study the hypothesis that hyperbaric oxygen therapy (HBOT) both improves the adhesion molecules levels and antioxidant capacity. Methods: Thirty blood samples from ten patients after acute TBI were obtained after injury and before and after HBOT. Four patients received early HBOT started two weeks after injury, four patients received late HBOT started ten weeks after injury and two patients did not receive HBOT and served as control in this study. The HBOT patients received total 30 times HBOT in six weeks period. Results: Those serum biomarkers in patients with TBI had not significantly difference in glutathione (GSH), thiobarbituric acid reactive substances (TBARS), soluble intercellular cell adhesion-molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations on admission between early HBOT, late HBOT, and control group (p = 0.916, p = 0.98, p = 0.306, and p = 0.548, respectively). Serum GSH levels were higher at 10 weeks after injury in the early HBOT group than in the late HBOT group and control group (mean, 1.40 μmol/L, 1.16 μmol/L, and 1.05 μmol/L, respectively). Then the serum GSH level was increased at 18 weeks after injury in the late HBOT group (mean, 1.49 μmol/L). However, there was only statistically significant difference at Weeks 18 (p = 0.916, p = 0.463, and p = 0.006, at Week 2, Week 10, and Week 18, respectively). Serum TBARS levels were decreased at 10 weeks after injury in the early HBOT group than in the late HBOT group and control group (mean, 11.21 μmol/L, 17.23 μmol/L, and 17.14 μmol/L, respectively). Then the serum TBARS level was decreased at 18 weeks after injury in the late HBOT group (mean, 12.06 μmol/L). There was statistically significant difference after HBOT (p = 0.98, p = 0.007, and p = 0.018, at Week 2, Week 10, and Week 18, respectively). There was no statistically significant difference between the three groups on sICAM-1 and sVCAM-1 levels from Week 2 to Week 18. Conclusions: HBOT can improve serum oxidative stress in patients after TBI. These molecules may be added as evaluation markers in clinical practice. Perhaps in the future it may also become part of the treatment of patients after acute traumatic brain injury. Further large-scale study may be warrant.

Intracerebral Iron Accumulation may be Associated with Secondary Brain Injury in Patients with Poor Grade Subarachnoid Hemorrhage

BackgroundThe amount of intracranial blood is a strong predictor of poor outcome after subarachnoid hemorrhage (SAH). Here, we aimed to measure iron concentrations in the cerebral white matter, using the cerebral microdialysis (CMD) technique, and to associate iron levels with the local metabolic profile, complications, and functional outcome.MethodsFor the observational cohort study, 36 patients with consecutive poor grade SAH (Hunt & Hess grade of 4 or 5, Glasgow Coma Scale Score ≤ 8) undergoing multimodal neuromonitoring were analyzed for brain metabolic changes, including CMD iron levels quantified by graphite furnace atomic absorption spectrometry. The study time encompassed 14 days after admission. Statistical analysis was performed using generalized estimating equations.ResultsPatients were admitted in a poor clinical grade (n = 26, 72%) or deteriorated within 24 h (n = 10, 28%). The median blood volume in the subarachnoid space was high (SAH sum score = 26, interquartile range 20–28). Initial CMD iron was 44 µg/L (25–65 µg/L), which significantly decreased to a level of 25 µg/L (14–30 µg/L) at day 4 and then constantly increased over the remaining neuromonitoring days (p < 0.01). A higher intraventricular hemorrhage sum score (≥ 5) was associated with higher CMD iron levels (Wald-statistic = 4.1, df = 1, p = 0.04) but not with the hemorrhage load in the subarachnoid space (p = 0.8). In patients developing vasospasm, the CMD iron load was higher, compared with patients without vasospasm (Wald-statistic = 4.1, degree of freedom = 1, p = 0.04), which was not true for delayed cerebral infarction (p = 0.4). Higher iron concentrations in the brain extracellular fluid (34 µg/L, 36–56 µg/L vs. 23 µg/L, 15–37 µg/L) were associated with mitochondrial dysfunction (CMD lactate to pyruvate ratio > 30 and CMD-pyruvate > 70 µM/L, p < 0.001). Brain extracellular iron load was not associated with functional outcome after 3 months (p > 0.5).ConclusionsThis study suggests that iron accumulates in the cerebral white matter in patients with poor grade SAH. These findings may support trials aiming to scavenger brain extracellular iron based on the hypothesis that iron-mediated neurotoxicity may contribute to acute and secondary brain injury following SAH.